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Differential regulation of germ line apoptosis and germ cell differentiation by CPEB family members in C. elegans.


ABSTRACT: Cytoplasmic polyadenylation element binding (CPEB) proteins are evolutionary conserved RNA-binding proteins that control mRNA polyadenylation and translation. Orthologs in humans and other vertebrates are mainly involved in oogenesis. This is also the case for the C. elegans CPEB family member CPB-3, whereas two further CPEB proteins (CPB-1 and FOG-1) are involved in spermatogenesis. Here we describe the characterisation of a new missense allele of cpb-3 and show that loss of cpb-3 function leads to an increase in physiological germ cell death. To better understand the interaction and effect of C. elegans CPEB proteins on processes such as physiological apoptosis, germ cell differentiation, and regulation of gene expression, we characterised changes in the transcriptome and proteome of C. elegans CPEB mutants. Our results show that, despite their sequence similarities CPEB family members tend to have distinct overall effects on gene expression (both at the transcript and protein levels). This observation is consistent with the distinct phenotypes observed in the various CPEB family mutants.

SUBMITTER: Singh KD 

PROVIDER: S-EPMC5536308 | biostudies-literature | 2017

REPOSITORIES: biostudies-literature

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Differential regulation of germ line apoptosis and germ cell differentiation by CPEB family members in C. elegans.

Singh Kapil Dev KD   Zheng Xue X   Milstein Stuart S   Keller Martin M   Roschitzki Bernd B   Grossmann Jonas J   Hengartner Michael O MO  

PloS one 20170731 7


Cytoplasmic polyadenylation element binding (CPEB) proteins are evolutionary conserved RNA-binding proteins that control mRNA polyadenylation and translation. Orthologs in humans and other vertebrates are mainly involved in oogenesis. This is also the case for the C. elegans CPEB family member CPB-3, whereas two further CPEB proteins (CPB-1 and FOG-1) are involved in spermatogenesis. Here we describe the characterisation of a new missense allele of cpb-3 and show that loss of cpb-3 function lead  ...[more]

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